共查询到20条相似文献，搜索用时 468 毫秒
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采用单因子法对影响免疫共沉淀结果的各因素进行优化.以hCLP46(human CAP10-like protein46)蛋白和内质网分子伴侣calnexin为例,对相互作用开展研究.通过对细胞裂解液各组分浓度、抗体用量、hCLP46的蛋白量和交联剂DSP因素的优化,验证了hCLP46(human CAP10-like protein46)蛋白和内质网分子伴侣calnexin间的弱相互作用.研究结果为探讨蛋白质之间弱相互作用提供一定的参考价值. 相似文献
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hCLP46(human CAP10-like protein46)是从MDS-AML患者的CD34+干细胞cDNA文库中筛选出的基因.我们利用串联亲和纯化技术来筛选与hCLP46有相互作用的蛋白.通过体内交联-甘氨酸洗脱策略,检测到7条有差异的蛋白带,经液相色谱-质谱联用鉴定,得到了CNX和PDI等一系列内质网伴侣蛋白.所以hCLP46可能是一个糖蛋白,其成熟过程利用了BiP/Grp94和CNX/CRT 2套伴侣蛋白系统. 相似文献
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Simona Cernea Minodora Dobreanu 《Biochemia medica : ?asopis Hrvatskoga dru?tva medicinskih biokemi?ara / HDMB》2013,23(3):266-280
Diabetes is a complex, heterogeneous condition that has beta cell dysfunction at its core. Many factors (e.g. hyperglycemia/glucotoxicity, lipotoxicity, autoimmunity, inflammation, adipokines, islet amyloid, incretins and insulin resistance) influence the function of pancreatic beta cells. Chronic hyperglycaemia may result in detrimental effects on insulin synthesis/secretion, cell survival and insulin sensitivity through multiple mechanisms: gradual loss of insulin gene expression and other beta-cell specific genes; chronic endoplasmic reticulum stress and oxidative stress; changes in mitochondrial number, morphology and function; disruption in calcium homeostasis. In the presence of hyperglycaemia, prolonged exposure to increased free fatty acids result in accumulation of toxic metabolites in the cells (“lipotoxicity”), finally causing decreased insulin gene expression and impairment of insulin secretion. The rest of the factors/mechanisms which impact on the course of the disease are also discusses in detail.The correct assessment of beta cell function requires a concomitant quantification of insulin secretion and insulin sensitivity, because the two variables are closely interrelated. In order to better understand the fundamental pathogenetic mechanisms that contribute to disease development in a certain individual with diabetes, additional markers could be used, apart from those that evaluate beta cell function.The aim of the paper was to overview the relevant mechanisms/factors that influence beta cell function and to discuss the available methods of its assessment. In addition, clinical considerations are made regarding the therapeutical options that have potential protective effects on beta cell function/mass by targeting various underlying factors and mechanisms with a role in disease progression. 相似文献
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Harish Rao B V. Govindaraju C. N. Manjunath 《Indian journal of clinical biochemistry : IJCB》2007,22(1):18-21
Majority of patients who experience a Coronary Heart disease event have one or more of the conventional risk factors for atherosclerosis
and so do many people who have not yet experienced such an event. Thus predictive models based on conventional risk factors
have lower than the desired accuracy, providing a stimulus to search for new factors to predict accurately the risk of CHD.
In this regard newer risk factors like homocysteine, Lp(a), insulin resistances are the important ones and are called as ‘novel
risk factors’. The study was undertaken to find the prediction of CHD risk by homocysteine in comparison with other conventional
risk factors. The data obtained suggests a very high sensitivity, specificity and accuracy with above 90% positive prediction
value for homocysteine in CHD patients when compared to commonest conventional risk factors. 相似文献
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Muthuswamy Balasubramanyam Raji Lenin Finny Monickaraj 《Indian journal of clinical biochemistry : IJCB》2010,25(2):111-118
The endoplasmic reticulum (ER) is a cellular compartment responsible for multiple important cellular functions including the
biosynthesis and folding of newly synthesized proteins destined for secretion, such as insulin. A myriad of pathological and
physiological factors perturb ER function and cause dysregulation of ER homeostasis, leading to ER stress. Accumulating evidence
suggests that ER stress plays a role in the pathogenesis of diabetes, contributing to pancreatic β-cell loss and insulin resistance.
ER stress may also link obesity, inflammation and insulin resistance in type 2 diabetes. In this review, we address the transition
from physiology to pathology, namely how and why the physiological UPR evolves to a proapoptotic ER stress response in diabetes
and its complications. Special attention was given to elucidate how ER stress could explain some of the ‘clinical paradoxes’
such as secondary sulfonylurea failure, initial worsening of retinopathy during tight glycemic control, insulin resistance
induced by protease inhibitors and other clinically relevant observations. 相似文献
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Pradeep Venkatesh Garg Satpal Lalit Verma Tewari Hem Kumar Sheena Garg 《Indian journal of clinical biochemistry : IJCB》2001,16(1):9-14
Antioxidants are a small group of substances that protect living cells from the destructive consequences of powerful oxidizing
intermediates that can be formed from oxygen. Situations in which pro-oxidant mechanisms within the body are more active than
the antioxidant mechanisms (oxidative stress) predispose and contribute to the pathogenesis of several ailments in various
organs of the body. In the eye, pro-oxidant factors have been blamed for the causation of diseases such as age related macular
degeneration and senile cataract. The role of pro-oxidants in the genesis of certain diseases is well established however,
the effectivity of antioxidants provided to the body by dietary supplementation is inconclusive. In this article we provide
a review on the basic concepts of antioxidant-pro-oxidant interaction in relation to its effects on the eye. 相似文献
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Rizwan Ahmad Anil K. Tripathi Payal Tripathi Ranjana Singh Sushma Singh Raj K. Singh 《Indian journal of clinical biochemistry : IJCB》2008,23(4):328-333
Chronic myeloid leukemia is a myeloproliferative disorder with a unique rearrangement, the Philadelphia chromosome. Oxidative
stress, a pervasive condition of an increased number of reactive oxygen species, is now recognized to be prominent feature
of various diseases and their progression. Thus antioxidants, which control the oxidative stress state, represent a major
line of defense regulating overall true state of health. The relationship between antioxidants status and levels of well-known
markers of oxidative stress that are measured as lipid peroxides and oxidized proteins reflect better health indices and postures.
The aim of this study was to evaluate the role of oxidative stress in pathophysiology of Chronic myeloid leukemia by measuring
the circulating plasma lipid peroxide levels in terms of malonyldialdehyde, total lipid hydroperoxide and oxidized proteins
as protein carbonyl whereas antioxidant status were estimated in terms of reduced glutathione and total thiol in plasma of
Chronic myeloid leukemia patients. The present study included 47 Chronic myeloid leukemia patients and 20 age-and sex-matched
healthy subjects. Out of 47 Chronic myeloid leukemia patients, 31 were in chronic phase (CML-CP) and 16 in accelerated phase
(CML-AP). The median age of Chronic myeloid leukemia patients was 33 years and that of controls was 32 years. Oxidative stress
and antioxidant status in plasma were evaluated by spectrophotometric procedures. There was a significant increase (p<0.05)
in plasma malonyldialdehyde, total lipid hydroperoxide and protein carbonyl levels in Chronic myeloid leukemia patients as
compared to healthy subjects. Our results also showed that plasma malonyldialdehyde and protein carbonyl levels were markedly
elevated (p<0.05) in both chronic phase (CML-CP) and accelerated phase (CML-AP) as compared to healthy volunteers. Antioxidant
status was found to be significantly decreased (p<0.05) in Chronic myeloid leukemia patients and its phases as compared to
healthy participants. It could be concluded that oxidative stress may be associated with the pathophysiology of Chronic myeloid
leukemia. 相似文献
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V. Govindaraju Neelam C. N. Manjunath H. Venkataramiah T. R. Raghu 《Indian journal of clinical biochemistry : IJCB》2003,18(1):8-14
Conclusion There is considerable epidemiological evidence, which confirms the importance of plasma homocysteine as a powerful predictor
of future risk of coronary heart disease and other complications of atherosclerosis. Treatment of hyperhomocysteinemia varies
with the underlying cause. However, an inexpensive vitamin supplementation with folic acid, vitamin B12 and vitamin B 6 is
generally effective in reducing homocysteine concentrations. Several randomised, controlled trials evaluating the effects
of folic acid based supplements on homocysteine concentrations have been conducted over the last decade. In most patients,
folic acid alone, and in combination of vitamin B12 and B6, has been shown to reduce homocysteine concentrations within four
to six weeks after the initiation of therapy (34).
However, no study has yet demonstrated that lowering of homocysteine by vitamin supplementation decreases the cardiovascular
morbidity or mortality. Avoidance of excessive meat intake and increased consumption of fresh vegetables and fruits is a dietary
measure, which has many health benefits, including a potential to reduce elevated homocysteine levels. The other reasonable
approach is to determine levels of fasting homocysteine in high risk patients and it may be advisable to increase their intake
of vitamin fortified foods and/or to suggest the daily use of supplemental vitamins. Several large scale randomised trials
like Heart Outcomes Prevention Evaluation (HOPE-2) Study, Mcmaster University, Canada, Study of the Effectiveness of Additional
Reductions in Cholesterol and Homocysteine (SERCH), Clinical Trial Service Unit, Oxford, U.K, Cambridge Heart Antioxidant
Study (CHAOS-2) University of Cambridge, U.K, Bergen Vitamin Study, University of Bergen Norway, Women's Antioxidant and Cardiovascular
Disease Study (WACS) Harvard Medical School, U.S.A, Prevention with a combined inhibitor and folate in Coronary Heart Disease
(PACIFIC) study, University of Sydney, Australia, and many others are ongoing to assess the effect of homocysteine—lowering
by vitamin supplementation on risk of vascular disease. 相似文献
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Farhana Zahir Shameem J Rizvi Soghra K Haq Rizwan H Khan 《Indian journal of clinical biochemistry : IJCB》2006,21(2):149-152
Mercury pollution and acute neurotoxicity of mercury is well known. The recent reports suggest the adverse effect of low dose
mercury, though the available literature is still silent on its mechanism. This study was therefore undertaken to probe the
effect of low dose methyl mercury induced heavy metal toxicity on free radical stress and its impact on behaviour of male
albino rats. Male albino rats were exposed to 1 mg/kg body wt of methylmercury chloride for seven days, on day 8 they were
tested for motor and memory functions. They were sacrificed later for biochemical estimations for rate of lipid peroxidation,
nucleic acids, proteins in cerebrum, cerebellum and brain stem. There was an increase in the rate of lipid peroxidation showing
methyl mercury induced free radical stress. The motor and memory functions demonstrated a clear decline, besides there was
a lowering in the levels of nucleic acids and proteins as compared to controls. The results are important in view of recent
reports that methyl mercury induced free radical stress results in early ageing and may serve as an initiating factor more
specifically for neurodegenerative disorders like Alzeihemer's disease and dementias. The current findings support the notion
that incorporating dietary antioxidants like curcumin, ascorbic acid and α-tocopherol in routine diet from early age may help
combat the risk of developing such disorders in ensuing years. 相似文献